Alterations in intracellular calcium following infection of human endothelial cells with Trypanosoma cruzi

Stephen A. Morris, Herbert Tanowitz, Victor Bernard Hatcher, John P. Bilezikian, Murray Wittner

Research output: Contribution to journalArticle

45 Citations (Scopus)

Abstract

Trypanosoma cruzi infection in cultured human umbilical vein endothelial cells increased basal cellular calcium levels from 55 to 110 nM, as monitored with the fluorescent probe, fura-2. It also influenced intracellular calcium such that consistently higher total levels were observed in response to bradykinin, angiotensin II and norepinephrine, as compared to similarly treated uninfected cells. However, bradykinin and angiotensin II-dependent increases in calcium, when considered as the absolute increment or fold elevation over basal, were significantly lower in infected endothelial cells. Infection also influenced changes in calcium levels due to agents that operate independently of plasma membrane receptors. In the presence of ionomycin, the magnitude and rate of rise of intracellular calcium were decreased; additionally the calcium peak was delayed and the subsequent decline slowed. Similar to the results with bradykinin and angiotensin II, infection decreased both the increment in and fold stimulation of intracellular calcium in response to ionomycin. In contrast, infection altered only the total calcium stimulated in response to oligomycin; neither the fold stimulation of, nor increment in intracellular calcium was affected. These results indicate that (1) infection by T. cruzi alters calcium homeostasis in endothelial cells under basal and stimulated conditions; (2) both receptor-dependent and receptor-independent mechanisms are affected by infection. The possible contribution of altered calcium homeostasis induced by T. cruzi in the pathogenesis of chagasic cardiomyopathy is considered.

Original languageEnglish (US)
Pages (from-to)213-221
Number of pages9
JournalMolecular and Biochemical Parasitology
Volume29
Issue number2-3
DOIs
StatePublished - 1988

Fingerprint

Trypanosoma cruzi
Endothelial Cells
Calcium
Infection
Bradykinin
Angiotensin II
Ionomycin
Homeostasis
Oligomycins
Fura-2
Human Umbilical Vein Endothelial Cells
Cardiomyopathies
Fluorescent Dyes
Norepinephrine
Cell Membrane

Keywords

  • Endothelial cell
  • Intracellular calcium
  • Trypanosoma cruzi

ASJC Scopus subject areas

  • Molecular Biology
  • Parasitology

Cite this

Alterations in intracellular calcium following infection of human endothelial cells with Trypanosoma cruzi. / Morris, Stephen A.; Tanowitz, Herbert; Hatcher, Victor Bernard; Bilezikian, John P.; Wittner, Murray.

In: Molecular and Biochemical Parasitology, Vol. 29, No. 2-3, 1988, p. 213-221.

Research output: Contribution to journalArticle

Morris, Stephen A. ; Tanowitz, Herbert ; Hatcher, Victor Bernard ; Bilezikian, John P. ; Wittner, Murray. / Alterations in intracellular calcium following infection of human endothelial cells with Trypanosoma cruzi. In: Molecular and Biochemical Parasitology. 1988 ; Vol. 29, No. 2-3. pp. 213-221.
@article{299a7f025c1042d8acc096c853f502c8,
title = "Alterations in intracellular calcium following infection of human endothelial cells with Trypanosoma cruzi",
abstract = "Trypanosoma cruzi infection in cultured human umbilical vein endothelial cells increased basal cellular calcium levels from 55 to 110 nM, as monitored with the fluorescent probe, fura-2. It also influenced intracellular calcium such that consistently higher total levels were observed in response to bradykinin, angiotensin II and norepinephrine, as compared to similarly treated uninfected cells. However, bradykinin and angiotensin II-dependent increases in calcium, when considered as the absolute increment or fold elevation over basal, were significantly lower in infected endothelial cells. Infection also influenced changes in calcium levels due to agents that operate independently of plasma membrane receptors. In the presence of ionomycin, the magnitude and rate of rise of intracellular calcium were decreased; additionally the calcium peak was delayed and the subsequent decline slowed. Similar to the results with bradykinin and angiotensin II, infection decreased both the increment in and fold stimulation of intracellular calcium in response to ionomycin. In contrast, infection altered only the total calcium stimulated in response to oligomycin; neither the fold stimulation of, nor increment in intracellular calcium was affected. These results indicate that (1) infection by T. cruzi alters calcium homeostasis in endothelial cells under basal and stimulated conditions; (2) both receptor-dependent and receptor-independent mechanisms are affected by infection. The possible contribution of altered calcium homeostasis induced by T. cruzi in the pathogenesis of chagasic cardiomyopathy is considered.",
keywords = "Endothelial cell, Intracellular calcium, Trypanosoma cruzi",
author = "Morris, {Stephen A.} and Herbert Tanowitz and Hatcher, {Victor Bernard} and Bilezikian, {John P.} and Murray Wittner",
year = "1988",
doi = "10.1016/0166-6851(88)90076-X",
language = "English (US)",
volume = "29",
pages = "213--221",
journal = "Molecular and Biochemical Parasitology",
issn = "0166-6851",
publisher = "Elsevier",
number = "2-3",

}

TY - JOUR

T1 - Alterations in intracellular calcium following infection of human endothelial cells with Trypanosoma cruzi

AU - Morris, Stephen A.

AU - Tanowitz, Herbert

AU - Hatcher, Victor Bernard

AU - Bilezikian, John P.

AU - Wittner, Murray

PY - 1988

Y1 - 1988

N2 - Trypanosoma cruzi infection in cultured human umbilical vein endothelial cells increased basal cellular calcium levels from 55 to 110 nM, as monitored with the fluorescent probe, fura-2. It also influenced intracellular calcium such that consistently higher total levels were observed in response to bradykinin, angiotensin II and norepinephrine, as compared to similarly treated uninfected cells. However, bradykinin and angiotensin II-dependent increases in calcium, when considered as the absolute increment or fold elevation over basal, were significantly lower in infected endothelial cells. Infection also influenced changes in calcium levels due to agents that operate independently of plasma membrane receptors. In the presence of ionomycin, the magnitude and rate of rise of intracellular calcium were decreased; additionally the calcium peak was delayed and the subsequent decline slowed. Similar to the results with bradykinin and angiotensin II, infection decreased both the increment in and fold stimulation of intracellular calcium in response to ionomycin. In contrast, infection altered only the total calcium stimulated in response to oligomycin; neither the fold stimulation of, nor increment in intracellular calcium was affected. These results indicate that (1) infection by T. cruzi alters calcium homeostasis in endothelial cells under basal and stimulated conditions; (2) both receptor-dependent and receptor-independent mechanisms are affected by infection. The possible contribution of altered calcium homeostasis induced by T. cruzi in the pathogenesis of chagasic cardiomyopathy is considered.

AB - Trypanosoma cruzi infection in cultured human umbilical vein endothelial cells increased basal cellular calcium levels from 55 to 110 nM, as monitored with the fluorescent probe, fura-2. It also influenced intracellular calcium such that consistently higher total levels were observed in response to bradykinin, angiotensin II and norepinephrine, as compared to similarly treated uninfected cells. However, bradykinin and angiotensin II-dependent increases in calcium, when considered as the absolute increment or fold elevation over basal, were significantly lower in infected endothelial cells. Infection also influenced changes in calcium levels due to agents that operate independently of plasma membrane receptors. In the presence of ionomycin, the magnitude and rate of rise of intracellular calcium were decreased; additionally the calcium peak was delayed and the subsequent decline slowed. Similar to the results with bradykinin and angiotensin II, infection decreased both the increment in and fold stimulation of intracellular calcium in response to ionomycin. In contrast, infection altered only the total calcium stimulated in response to oligomycin; neither the fold stimulation of, nor increment in intracellular calcium was affected. These results indicate that (1) infection by T. cruzi alters calcium homeostasis in endothelial cells under basal and stimulated conditions; (2) both receptor-dependent and receptor-independent mechanisms are affected by infection. The possible contribution of altered calcium homeostasis induced by T. cruzi in the pathogenesis of chagasic cardiomyopathy is considered.

KW - Endothelial cell

KW - Intracellular calcium

KW - Trypanosoma cruzi

UR - http://www.scopus.com/inward/record.url?scp=0023890817&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023890817&partnerID=8YFLogxK

U2 - 10.1016/0166-6851(88)90076-X

DO - 10.1016/0166-6851(88)90076-X

M3 - Article

VL - 29

SP - 213

EP - 221

JO - Molecular and Biochemical Parasitology

JF - Molecular and Biochemical Parasitology

SN - 0166-6851

IS - 2-3

ER -